ライフサイエンスコーパス: SMC

1 SMC (structural maintenance of chromosomes) family membe

2 SMC complexes include three major classes: cohesin, cond

3 SMC consisted of education, toilet training, and laxativ

4 SMC contractile gene expression and, thus differentiatio

5 SMC growth in a xenograft assay was driven by progestero

6 SMC in older children is well tolerated and effective an

7 SMC phenotypes can be altered during pathological vascul

8 SMC substantially reduced the incidence of outpatient ca

9 SMC was delivered by specialist doctors but was not stan

10 SMC was introduced into three districts over three years

11 SMC was well tolerated with no serious adverse reactions

12 SMC++ can jointly infer population size histories and sp

13 SMC-derived AdvSca1 cells exhibit a multipotent phenotyp

14 SMC-Nampt knockout mice were viable but with mildly dila

15 SMCs also regulate several immunomodulatory properties w

16 SMCs are thought to accumulate in plaques because fully

17 SMCs were not apoptotic but displayed senescence associa

18 in ICC-IM followed by conduction to adjacent SMCs where phasic calcium entry through CavL sums to pro

19 aling, presence of specific neural crest and SMC markers, expression of VEGF-D and female sex hormone

20 tion potentiated H2O2-induced DNA damage and SMC apoptosis.

21 n 1 (XBP1) plays an important role in EC and SMC cellular functions.

22 reductions in SMC numbers within lesions and SMC investment within the fibrous cap, which may result

23 TGFbeta/Smad3-stimulated KLF5 production and SMC de-differentiation were blocked by resveratrol via i

24 ated Kruppel-like factor (KLF5) protein, and SMC de-differentiation which was reversed by KLF5 siRNA.

25 and demonstrated that iPSC reprogramming and SMC lineage differentiation of somatic patient cells wit

26 effect correlated with oxidative stress and SMC apoptosis.

27 erstanding of communications between ECs and SMCs via micro-RNA.

28 stimulator for switching the anti-angiogenic SMC phenotype to the pro-angiogenic phenotype, which may

29 at synthetic SMC exhibits an anti-angiogenic SMC phenotype, whereas contractile SMC shows a pro-angio

30 preexisting SMCs give rise to excess aortic SMCs in elastin mutants, and these SMCs are hyperprolife

31 However, a role for Nampt in aortic SMCs in vivo is unknown.

32 mutations lead to a reduced number of aortic SMCs during development and increased SMC apoptosis in t

33 as been proposed that the response of aortic SMCs to the hemodynamic load on a structurally defective

34 the nucleus in SMCs, especially in apoptotic SMCs.

35 We apply SMC++ to analyze sequence data from over a thousand huma

36 TLR7 deficiency also reduced aortic arch SMC loss and lesion intima and media cell apoptosis.

37 In arterial SMCs, CXCR4 sustained normal vascular reactivity and con

38 of membrane potential is complicated because SMC are electrically coupled to interstitial cells of Ca

39 in MED12, suggesting an interaction between SMC and TAF to coordinate their growth.

40 T, revealing an inverse relationship between SMC NAMPT content and aortic diameter.

41 in older children that could be prevented by SMC.

42 assigned to receive specialist medical care (SMC) alone (control group) or SMC with additional guided

43 hysiotherapy (PPT) vs standard medical care (SMC) in children with FC.

44 nclude Theta via the sequential Monte Carlo (SMC) samplers for static models.

45 We report a "cationic" SMC method using a PAd3-Pd catalyst that proceeds at rt

46 was directly involved in smooth muscle cell (SMC) apoptosis.

47 in is a key regulator of smooth muscle cell (SMC) calcification via its recruitment to extracellular

48 Vascular smooth muscle cell (SMC) composes the majority of the vascular wall and reta

49 c disease either disrupt smooth muscle cell (SMC) contraction or adherence to an impaired extracellul

50 rgets in human and mouse smooth muscle cell (SMC) cultures.

51 Smooth muscle cell (SMC) death contributes to plaque destabilization.

52 Foxe3 deficiency reduced smooth muscle cell (SMC) density and impaired SMC differentiation in the asc

53 Smooth muscle cell (SMC) differentiation is essential for vascular developme

54 proaches combined with a smooth muscle cell (SMC) epigenetic lineage mark, we report that a subpopula

55 proaches combined with a smooth muscle cell (SMC) epigenetic lineage mark, we report that a subpopula

56 mary human aortic single smooth muscle cell (SMC) forces using nanonet force microscopy in both insid

57 andable cell lines under smooth muscle cell (SMC) growth conditions that retained a patient-specific

58 ferentiation towards the smooth muscle cell (SMC) lineage but not in combination.

59 rked changes in vascular smooth muscle cell (SMC) phenotype and function.

60 Smooth muscle cell (SMC) phenotypic conversion from a contractile to a migra

61 Vascular smooth muscle cell (SMC) proliferation and endothelial cell (EC) dysfunction

62 xpression and neointimal smooth muscle cell (SMC) proliferation were assessed by immunohistochemistry

63 ic ApoE(-/-) mice; also, smooth muscle cell (SMC), macrophage and leukocyte abundance was prevented c

64 Here we demonstrate that smooth muscle cell (SMC)-specific conditional knockout of Oct4 in Apoe(-/-)

65 (T2)-driven)-specific or smooth muscle cell (SMC, SmmhcCreER(T2)- or TaglnCre-driven)-specific defici

66 dent Ca(2+) channels in smooth muscle cells (SMC) provide the Ca(2+) that triggers contraction.

67 eration of human venous smooth muscle cells (SMC) was measured by a DNA-binding assay, and ii) lipopo

68 -uterine leiomyoma were smooth muscle cells (SMC) with HMGA2 overexpression.

69 erved in ICC but not in smooth muscle cells (SMC).

70 Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) are in close contact w

71 ration and migration of smooth muscle cells (SMCs) and promoted the tube formation from ECs.

72 rentiates into vascular smooth muscle cells (SMCs) around those aortic arches destined for survival a

73 Vascular smooth muscle cells (SMCs) can resist and repair artery damage, but their cap

74 ing protein ARHGAP42 in smooth muscle cells (SMCs) controls blood pressure by inhibiting RhoA-depende

75 Smooth muscle cells (SMCs) in normal blood vessels exist in a highly differen

76 resolved in ICC but not smooth muscle cells (SMCs) in the IAS and rectum.

77 Loss and dysfunction of smooth muscle cells (SMCs) in the vasculature may cause defects associated wi

78 on into fibroblasts and smooth muscle cells (SMCs) is also described.

79 mice, MR deficiency in smooth muscle cells (SMCs) protected against kidney IR injury.

80 Our MFS-hiPSC-derived smooth muscle cells (SMCs) recapitulated the pathology seen in Marfan aortas,

81 ion in primary vascular smooth muscle cells (SMCs) that were isolated from renal vessels.

82 in vitro model, primary smooth muscle cells (SMCs) were stimulated with elevated transforming growth

83 phenotypically distinct smooth muscle cells (SMCs) within the rat anorectrum, we identified miRNA-139

84 ression in macrophages, smooth muscle cells (SMCs), and endothelial cells from mouse atherosclerotic

85 of elastic lamellae and smooth muscle cells (SMCs), and many arterial diseases are characterized by d

86 ne induced autophagy in smooth muscle cells (SMCs); further, it exhibited therapeutic potential for r

87 nduced proliferation of smooth muscle cells (SMCs); however, this phenotype could be reversed by knoc

88 Structural maintenance of chromosomes (SMC) complexes play critical roles in chromosome dynamic

89 The Structural Maintenance of Chromosomes (SMC) complexes: cohesin, condensin and Smc5/6 are involv

90 ntial Structural Maintenance of Chromosomes (SMC) complexes: cohesin, condensin, and Smc5/6.

91 in, a structural maintenance of chromosomes (SMC) family member.

92 The structural maintenance of chromosomes (SMC) family of proteins supports mitotic proliferation,

93 that structural-maintenance-of-chromosomes (SMC) complexes such as condensin and cohesin are involve

94 ates that are poorly compatible with classic SMC conditions, undergo clean coupling.

95 ar idea to the sequential Markov coalescent (SMC)-an approximation of the coalescent with crossover r

96 The Escherichia coli SMC complex, MukBEF, forms clusters of molecules that in

97 ltiple linear regression analysis to compare SMC with GES, adjusting for baseline and stratification

98 antagonists, called Smac mimetic compounds (SMCs), sensitize tumours to TNF-alpha-induced killing wh

99 somal organization by mutating the condensin SMC, by CRISPR/Cas9-mediated chromosome cutting, or by p

100 Interestingly, CPEC-conditioned SMC culture medium promoted EC proliferation and migrati

101 on and migration induced by CPEC-conditioned SMC medium.

102 e element binding protein and, consequently, SMC redifferentiation.

103 l barrier function, and a normal contractile SMC phenotype.

104 ngiogenic SMC phenotype, whereas contractile SMC shows a pro-angiogenic phenotype.

105 es because fully differentiated, contractile SMCs reprogramme into a 'synthetic' migratory phenotype,

106 The highly elongated, contractile SMCs initially rounded up, for 1-3 days, before spreadin

107 ation of the transition of fully contractile SMCs to a non-contractile, migratory phenotype with phag

108 SMCs and its target genes activation control SMC differentiation.

109 ifferent shapes, alignments, and correlating SMC marker levels were generated by varying strain, leng

110 ium-catalyzed Suzuki-Miyaura cross-coupling (SMC) reaction of Fmoc-protected bromo- or iodophenylalan

111 icates their use in Suzuki-Miyaura coupling (SMC) because a base is generally required for catalysis.

112 beta-Catenin-deficient SMCs show no change in p53 levels, but greater p53 acety

113 aortic integrity, mice with Nampt-deficient SMCs were generated.

114 The patient-derived SMC lines we have developed thus represent a novel cellu

115 induced pluripotent stem cell (iPSC)-derived SMCs from an HGPS patient.

116 In addition, SVAS iPSC-derived SMCs and the aortic media of elastin mutant mice and SVA

117 ascular progenitor cells from differentiated SMCs is a normal physiological process that contributes

118 lls is generated in situ from differentiated SMCs.

119 lls is generated in situ from differentiated SMCs.

120 ambiguously identified, fully differentiated SMCs.

121 transcription factor Klf4 in differentiated SMCs is essential for SMC reprogramming in vivo, whereas

122 uggest that the AS program in differentiated SMCs is orchestrated by the combined influence of auxili

123 itor-like properties and that differentiated SMCs are a source to varying degrees of each subpopulati

124 criptome changes in mouse de-differentiating SMCs and observed changes in hundreds of AS events.

125 at modulates TGF-beta/Smad3 signaling during SMC differentiation.

126 However, whether XBP1 is involved in EC-SMC interaction remains unclear.

127 aracterized by defective lamellae and excess SMCs; however, a mechanism linking these pathological fe

128 ubpopulations of progenitor cells expressing SMC, myeloid, and hematopoietic progenitor-like properti

129 n laminae and abundant alphaActin-expressing SMCs.

130 in the presence of multiple growth factors, SMC undergo a phenotype switch characterized by the loss

131 sin and other members of the protein family (SMC [structural maintenance of chromosomes]) and their r

132 For SMC populations, we measured the I-O and O-I forces to b

133 Klf4 in differentiated SMCs is essential for SMC reprogramming in vivo, whereas in vitro approaches d

134 SMCs, suggesting miR-150 is responsible for SMC-stimulated EC migration.

135 Furthermore, SMC calcification required Rab11-dependent trafficking a

136 nts showed that the newly formed beta-gal(+) SMC were not derived from circulating bone marrow-derive

137 nd neointimal growth, and evidence of higher SMC mitochondrial respiration.

138 However, how SMC phenotypes affect EC properties remains largely unkn

139 It remains unclear how SMCs structure chromosomes and how their mechanochemical

140 Human SMCs are first dedifferentiated for 4 days to achieve a

141 d deletion of this element in cultured human SMCs markedly reduced endogenous ARHGAP42 expression.

142 f the feasibility of the conversion of human SMCs towards endothelial lineage through an intermediate

143 Hence, MLCK activation in IAS-SMCs caused by a global rise in [Ca(2+)]i via a RyR-TMEM

144 scle cells from internal anal sphincter (IAS-SMCs) abolishes basal tone, impairing defecation.

145 mooth muscle cell (SMC) density and impaired SMC differentiation in the ascending aorta.

146 fibrous cap, which may result from impaired SMC migration.

147 In the first year of implementation, SMC was delivered to children aged 3-59 months; the age

148 malaria, with 64 in control areas and 59 in SMC areas, showing a reduction in the incidence rate of

149 Fragments of Fat1 accumulate in SMC mitochondria, and the Fat1 intracellular domain inte

150 A similar current was not available in SMC.

151 various cellular events, their functions in SMC differentiation remain largely unknown.

152 pated in formation of microcalcifications in SMC culture.

153 KATP is a conductance prominent in SMC.

154 probably the result of marked reductions in SMC numbers within lesions and SMC investment within the

155 tion, and downstream signaling, resulting in SMC misalignment and hyperproliferation.

156 hoA, Rac1, and Cdc42) play a central role in SMC functions including migration, proliferation, and co

157 mia at the end of the transmission season in SMC areas were 68% (95% CI 35%-85%) p = 0.002 in 2008, 8

158 tality, the primary endpoint, was similar in SMC and control areas (4.6 and 4.5 per 1000 respectively

159 ated cationic pathway for transmetalation in SMC.

160 Ectopic overexpression of let-7 in SMCs inhibited inflammatory responses including prolifer

161 thin the dilated human thoracic aorta and in SMCs cultured from these tissues, which inversely correl

162 e discovered unrepaired DNA strand breaks in SMCs within the human ascending aorta, which were specif

163 emia models revealed that XBP1 deficiency in SMCs significantly attenuated angiogenesis in ischemic t

164 In vivo, Rac1 deletion in SMCs or pharmacological Rac1 inhibition by nebulization

165 g aorta, which were specifically enriched in SMCs with low NAMPT.

166 Gata6 is expressed in SMCs and its target genes activation control SMC differe

167 MR antagonism, or deletion of the MR gene in SMCs, limited the renal injury induced by IR through eff

168 acna1c expression was only 2-fold greater in SMCs than in ICC.

169 o SMCs to inhibit the expression of 5-HTT in SMCs and the proliferation of SMCs.

170 which was abolished by miR-150 knockdown in SMCs, suggesting miR-150 is responsible for SMC-stimulat

171 st, finerenone, or genetic deletion of MR in SMCs associated with weaker oxidative stress production.

172 Furthermore, genetic deletion of MR in SMCs blunted the production of Rac1-GTP after IR.

173 ess, ADAMTS-4 translocated to the nucleus in SMCs, especially in apoptotic SMCs.

174 ith sporadic ascending TAAD, particularly in SMCs.

175 long with decreased endostatin production in SMCs.

176 rol kidneys, and genetic deletion of Rac1 in SMCs protected against AKI.

177 Thus, integrin beta3-mediated signaling in SMCs links elastin deficiency and pathological stenosis,

178 ion of CGRP receptor proteins was similar in SMCs, RAMP1 associated with nuclear regions of endotheli

179 his study demonstrates that XBP1 splicing in SMCs can control EC migration via SMC derived EVs-mediat

180 ine whether a Nampt-NAD(+) control system in SMCs impacts aortic integrity, mice with Nampt-deficient

181 ression was 26.5-fold greater in ICC than in SMCs while Cacna1c expression was only 2-fold greater in

182 Thus in SMCs, the beta-catenin C-terminus indirectly represses p

183 using a let-7 mimic was tested: in vitro in SMCs using an endogenous anti-inflammatory lipid (lipoxi

184 and laxatives (n = 26), whereas PPT included SMC plus specific physiotherapeutic interventions (n = 2

185 aortic SMCs during development and increased SMC apoptosis in the ascending aorta in response to incr

186 Tracking the fate of individual SMCs is difficult as no specific markers of migratory SM

187 bited platelet-derived growth factor-induced SMC proliferation and protected SMCs from TNF-alpha-indu

188 injury-induced neointima formation, induced SMC redifferentiation.

189 Our findings indicate that ADAMTS-4 induces SMC apoptosis, degrades versican, promotes inflammatory

190 lesions of TA by exacerbating inflammation, SMC proliferation, and infiltration of pathogenic T cell

191 that has been reported previously to inhibit SMC proliferation and injury-induced neointima formation

192 eutic potential for restenosis by inhibiting SMC accumulation in a rat restenosis model.

193 ithelial transition is requisite to initiate SMCs reprogramming into vascular progenitors and that me

194 After vascular injury, SMC-derived AdvSca1 cells expand in number and are major

195 prevented PW1(+) cells differentiation into SMC but did not inhibit their proliferation.

196 Here, we find that embryos lacking SMC beta-catenin suffer impaired arterial maturation and

197 phenotype, the occurrence of macrophage-like SMCs in the lesions, and impaired cholesterol efflux.

198 pable of differentiating in vivo into mature SMCs, resident macrophages, and endothelial-like cells.

199 Neointimal SMC proliferation and medial SMC matrix metalloproteinase 9 expression were not alter

200 ly, in inhibition of TGF-beta/Smad3-mediated SMC differentiation.

201 steine sulfoxide (alliin), S-methylcysteine (SMC), and S-ethylcysteine (SEC).

202 arker) expression were reduced while SM-MHC (SMC contractile marker) levels were increased.

203 However, migratory SMCs did not uptake acetylated low-density lipoprotein o

204 ifficult as no specific markers of migratory SMCs exist.

205 egulation of TNF and IL-6 in human and mouse SMC cultures inversely correlated with A20 expression.

206 alignment, and expression of smooth muscle (SMC) differentiation markers, as those have been associa

207 tigates pathological aortic muscularization, SMC misorientation, and lumen loss and extends survival,

208 Neointimal SMC proliferation and medial SMC matrix metalloproteinas

209 In addition, Nf1(+/-) SMCs, which express CCR2, demonstrate an enhanced prolif

210 e; the overall mortality rate ratio [SMC: no SMC] was 0.90, 95% CI 0.68-1.2, p = 0.496).

211 consisted of similar numbers of SMC and non-SMC, which were mostly tumor-associated fibroblasts (TAF

212 to test the feasibility of the conversion of SMC into functional EC through the use of reprogramming

213 y was done to determine the effectiveness of SMC in Senegalese children up to ten years of age.

214 ockdown of GAS5 increased, the expression of SMC contractile proteins.

215 t in a significantly increased expression of SMC markers, compared to non-stretched controls.

216 l efflux from macrophages, and expression of SMC phenotypic markers.

217 entiate state characterized by expression of SMC-specific contractile proteins ("contractile phenotyp

218 Nine started implementation of SMC in 2008, 18 in 2009, and a further 18 in 2010, with

219 uman and mouse arteries, and inactivation of SMC Fat1 in mice potentiates the response to vascular da

220 Conversely, inhibition of SMC FGF signaling induces TGFbeta signaling converting p

221 In conclusion, loss of SMC-Tgfbr1 triggers multiple deleterious pathways, inclu

222 st, MED12-LM consisted of similar numbers of SMC and non-SMC, which were mostly tumor-associated fibr

223 The proliferation of SMC was inhibited in the presence of media conditioned b

224 Results of SMC-lineage-tracing studies showed that these effects we

225 Suppression of SMC apoptosis by maintenance of nuclear GAPDH/Ape1 inter

226 gene promoters, resulting in suppression of SMC marker gene transcription and, consequently, in inhi

227 95 in the regulation of the proliferation of SMCs through 5-HTT, which will contribute to a better un

228 on of 5-HTT in SMCs and the proliferation of SMCs.

229 In vitro, the effects of RR6 on SMC proliferation (water-soluble tetrazolium-1 assay) an

230 medical care (SMC) alone (control group) or SMC with additional guided graded exercise self-help (GE

231 4 in arterial endothelial cells (n=12-15) or SMCs (n=13-24) markedly increased atherosclerotic lesion

232 ive subunit interfaces absent from the other SMC complexes; an unusual 'molecular latch' and a functi

233 evels were reduced in atherosclerotic plaque SMCs, and this effect correlated with oxidative stress a

234 iments demonstrate that multiple preexisting SMCs give rise to excess aortic SMCs in elastin mutants,

235 to protect against DNA damage and premature SMC senescence, with relevance to human thoracic aortopa

236 Here we present SMC++, a new statistical tool capable of analyzing order

237 activity, reduced DNA damage, and prevented SMC apoptosis.

238 In primary SMCs, p66Shc restricted the activation of transient rece

239 s TGFbeta signaling converting proliferating SMCs to the contractile phenotype, even in the presence

240 Furthermore, Gata6 is sufficient to promote SMCs differentiation in vivo, and drive preservation of

241 The proposed SMC algorithm is evaluated on simulated DNA sequence dat

242 the accuracy of the estimates, the proposed SMC method shows a comparable and sometimes, better perf

243 xpression decreased DNA damage and protected SMCs against apoptosis.

244 ctor-induced SMC proliferation and protected SMCs from TNF-alpha-induced apoptosis.

245 rs of age; the overall mortality rate ratio [SMC: no SMC] was 0.90, 95% CI 0.68-1.2, p = 0.496).

246 in adults and in children too old to receive SMC was reduced by 26% (95% CI 18%-33%, p < 0.001) and t

247 PPT and for 63.0% of the children receiving SMC (adjusted odds ratio for success of PPT, 11.7; 95% c

248 receiving PPT vs 33.3% of subjects receiving SMC) (P < .001).

249 In vitro, RR6 reduced SMC proliferation and apoptosis that was not confirmed i

250 only the noncanonical p38 pathway regulated SMC apoptosis, a pathological mechanism also governed by

251 wever, the mechanisms dynamically regulating SMC phenotype are not fully defined.

252 existence of a novel population of resident SMC progenitor cells expressing PW1 and participating in

253 Resident SMCs may provide a potential source of macrophages in va

254 om binding to SBE DNA in TGF-beta-responsive SMC gene promoters, resulting in suppression of SMC mark

255 Each complex is scaffolded by a specific SMC protein dimer (heterodimer in eukaryotes) held toget

256 The specific SMC deletion or pharmacological inhibition of Rac1 in mi

257 e ARHGAP42 SNP rs604723 that exhibits strong SMC-selective, allele-specific activity.

258 icroscopy to visualize how Bacillus subtilis SMC (BsSMC) interacts with flow-stretched DNAs.

259 In the bacterium Bacillus subtilis, SMC-condensin complexes are topologically loaded at cent

260 ided proof of a novel concept that synthetic SMC exhibits an anti-angiogenic SMC phenotype, whereas c

261 udy, we found that PDGF-BB-induced synthetic SMCs suppressed EC proliferation and migration while exh

262 hildren with FC, PPT was more effective than SMC on all outcomes measured, with the exception of find

263 iews have been challenged, with reports that SMC phenotypic modulation may not occur during vascular

264 These results directly demonstrate that SMCs may rapidly undergo phenotypic modulation and devel

265 We report that SMCs synergize with innate immune stimulants and immune

266 The SMC-converted ECs exhibit typical endothelial markers ex

267 The SMC-derived EVs could trigger EC migration, which was ab

268 The SMC-derived miR-150-containing EVs or premiR-150 transfe

269 ifference, 4 [95% CI, 1-7]; P = .01) and the SMC Severity Grading Scale (median score, 2 vs 2; Hodges

270 y of this method is also demonstrated by the SMC reaction of bromophenylalanine-containing tripeptide

271 GAPDH bound Ape1 in the SMC nucleus, and blocking (or oxidation) of GAPDH active

272 ensin and cohesin, eukaryotic members of the SMC (structural maintenance of chromosomes)-kleisin prot

273 g antagonism is the primary regulator of the SMC phenotype switch.

274 We showed that the SMC algorithm for static model is a promising alternativ

275 Once spread, the SMCs became motile and displayed dynamic cell-cell commu

276 These SMC-derived progenitors are then differentiated along th

277 s the functional relationships between these SMC complexes.

278 ss aortic SMCs in elastin mutants, and these SMCs are hyperproliferative and dedifferentiated.

279 ch health post and of community attitudes to SMC were also undertaken.

280 no serious adverse reactions attributable to SMC drugs.

281 in DNA repair and cell survival), leading to SMC apoptosis.

282 10, CCL2, TNF, and IL-6 (mostly localized to SMC).

283 vesicles could transfer miR-195 from ECs to SMCs to inhibit the expression of 5-HTT in SMCs and the

284 tify Gata6-directed differentiation of NC to SMCs as an essential mechanism that specifies the aortic

285 her for inducing MSC differentiation towards SMCs without the addition of recombinant growth factors

286 for modulating the phenotype of MSCs towards SMCs that could easily be incorporated into currently av

287 y Eph-B4-positive endothelium and underlying SMC and infiltrating cells such as macrophages and leuko

288 s and the proportion of beta-gal(+) vascular SMC were increased, indicating a recruitment of PW1(+) c

289 is factor-alpha (TNF-alpha)-induced vascular SMC and EC activation was associated with reduced let-7

290 ells and their differentiation into vascular SMC during early chronic hypoxia-induced neomuscularizat

291 a novel antiapoptotic mechanism in vascular SMCs that involves interaction of nuclear glyceraldehyde

292 plicing in SMCs can control EC migration via SMC derived EVs-mediated miR-150 transfer and miR-150-dr

293 wing CrP treatment; also, PCNA and vimentin (SMC synthetic marker) expression were reduced while SM-M

294 In vivo, SMC p53 inactivation suppresses phenotypes caused by los

295 In areas where SMC was implemented, incidence of confirmed malaria in a

296 These data support a model in which SMC complexes function by processively enlarging DNA loo

297 at NCO sites and functions in parallel with SMC-5 to antagonize excess HR-based connections between

298 une checkpoint inhibitors when combined with SMCs.

299 the first evidence that ECs communicate with SMCs via micro-RNA195 in the regulation of the prolifera

300 tive response to MCP-1 when compared with WT SMCs.